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      • Nina F. Schor, M.D., Ph.D.
      • Richard G. Wyatt, M.D.
      • Janice Lee, D.D.S., M.D., M.S.
      • Andy Baxevanis, Ph.D.
      • Charles R. Dearolf, Ph.D.
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  • IRP Website
    • A premier environment where creative scientists conduct fundamental research for the betterment of human health – we are the IRP
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    • The NIH Research Festival is the showcase for intramural research
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    • A publication for and about the NIH intramural research community
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  • NIDB
    • The NIH Intramural Database collects and disseminates information about research being performed in the Intramural Programs
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2013–2014

WALS 2013–2014 season poster

An Afternoon with Poet Rita Dove: Sonata Mulattica

Rita Dove
-
Wednesday, March 13, 2013 at 3 p.m. ET
J. Edward Rall Cultural Lecture

Ms. Dove will discuss her latest book, Sonata Mulattica, a poetic treatise on the life of 19th-century Afro-European violinist George Polgreen Bridgetower. The son of a white woman and an “African Prince,” George Polgreen Bridgetower (1780–1860) travels to Vienna to meet “bad-boy” genius Ludwig van Beethoven. The great composer’s subsequent sonata is originally dedicated to the young mulatto, but George, exuberant with acclaim, offends Beethoven over a woman. From this crucial encounter evolves a grandiose yet melancholy poetic tale.

Neuromodulatory circuits and motivated behavior

Cori Bargmann, Ph.D.
The Rockefeller University
Monday, September 9, 2013 at 3 p.m. ET

Genetic variation, internal states, and environmental cues converge on shared neuronal circuits to regulate behaviors. In the nematode worm Caenorhabditis elegans, an anatomical wiring diagram provides an essential map for innate behaviors, such as preferences for specific stimuli. Superimposed on this detailed circuit diagram are neuromodulators reflecting internal states, which help select appropriate behavioral responses from a larger number of latent circuits, and lead to both rapid and long-lasting changes in behavior. Dr.

Proteoglycans: Arbiters of lipoprotein metabolism

Jeffrey D. Esko, Ph.D.
University of California, San Diego
Wednesday, September 11, 2013 at 3 p.m. ET

Recently, genetic experiments in mice identified the heparan sulfate proteoglycan syndecan-1 as an important receptor for the clearance of triglyceride-rich lipoprotein (TRL) in the liver. This binding site for the TRLs consists of a protein core and one or more heparan sulfate chains. Binding depends on the heparan sulfate chains based on the accumulation of plasma TRLs in mice bearing mutations in heparan sulfate biosynthesis. To identify the major apolipoproteins that mediate binding to the heparan sulfate chains, we developed a series of in vitro and in vivo assays.

Epidemiology: Back to translation

Moyses Szklo, M.D.
The Johns Hopkins University
Wednesday, September 25, 2013 at 3 p.m. ET
Robert S. Gordon Jr. Lecture

Epidemiology was born of the need to discover the evidence necessary for the practice of public health. Early generations of epidemiologists produced data with the objective of translating their findings into public health action. However, the need for epidemiology to establish its scientific credentials, and the fact that subsequent generations of epidemiologists lacked a public health background, eventually resulted in an almost exclusive focus on etiology.

Chromatin structure and the control of gene expression

Carl Wu, Ph.D.
Howard Hughes Medical Institute
Wednesday, October 30, 2013 at 3 p.m. ET
George Khoury Lecture

The Wu laboratory investigates the biochemical basis for histone H2A.Z exchange using the budding yeast model organism. They have identified the yeast SWR1 ATP-dependent chromatin remodeling complex as the responsible enzyme. In a purified system, SWR1 removes H2A-H2B dimers from nucleosomes and deposits free H2A.Z-H2B dimers in an ATP-dependent manner. Homologous enzymes have since been characterized in mammalian systems. How does SWR1 recognize promoters and enhancers genome-wide?

The structural basis of ebola viral pathogenesis

Erica Ollmann Saphire, Ph.D.
The Scripps Research Institute
Wednesday, November 6, 2013 at 3 p.m. ET
NIH Director’s Lecture

Dr. Saphire’s lab studies viruses with compact genomes that encode just four to seven genes each. Viruses with limited genomes offer a defined landscape of possible protein-protein interactions. Each protein is critical—many are obligated to perform multiple functions and some rearrange their structures to achieve those new functions. As a result, these few polypeptides accomplish a surprisingly complex set of biological functions including immune evasion, receptor recognition, cell entry, transcription, translation, assembly and exit. Dr.

Comprehensive molecular profiling to support treatment recommendations for advanced cancer

John D. Carpten, Ph.D.
TGen
Wednesday, November 13, 2013 at 3 p.m. ET

Prior to joining TGen, Dr. Carpten was an intramural tenure track investigator with the Cancer Genetics Branch of the National Human Genome Research Institute (NHGRI), NIH, a group that pioneered a number of innovative technologies and methods to study the underlying genetics of cancer. At NIH, he co-led the first published genome wide scan for prostate cancer susceptibility genes published in 1996 in Science. His lab subsequently discovered germ-line mutations in theRNASEL gene in HPC1-linked hereditary prostate cancer families.

The genetic basis of kidney cancer: targeting the metabolic basis of disease

W. Marston Linehan, M.D.
National Cancer Institute
Wednesday, November 20, 2013 at 3 p.m. ET
Astute Clinician Lecture

Dr. Linehan has had a long-standing interest in identification of the genetic basis of cancer of the kidney. Kidney cancer is not a single disease. It is made up of a number of different types of cancer, each of which has a different histology, a different clinical course, which respond differently to therapy and are caused by different genes. Studies of the kidney cancer gene pathways have revealed that kidney cancer is fundamentally a metabolic disease.

How bacteria and cancer cells regulate mutagenesis and their ability to evolve

Susan M. Rosenberg, Ph.D.
Baylor College of Medicine
Wednesday, December 4, 2013 at 3 p.m. ET

For 50 years the world believed that mutations occur at random. The discovery of stress-induced mutagenesis has changed ideas about mutation and evolution and revealed mutagenic programs that differ from standard spontaneous mutagenesis in rapidly proliferating cells. The stress-induced mutations occur during growth-limiting stress, and can include adaptive mutations that allow growth in the otherwise growth-limiting environment.

The protean manifestations of GATA2 deficiency across the lifespan

Steve M. Holland, M.D.
National Institute of Allergy and Infectious Diseases (NIAID)
Wednesday, December 11, 2013 at 3 p.m. ET
G. Burroughs Mider Lecture

GATA binding factor 2 (GATA2) was initially cloned in 1991 as a critical regulator of murine endothelial development, the complete absence of which was incompatible with life. Subsequent work confirmed that it was also critical for hematopoiesis, erythropoiesis, and macrophage function. After almost 20 years of characterization of patients with disseminated mycobacterial infections who had monocytopenia, B cell and NK (natural killer) cell cytopenia, Steve Holland’s group found heterozygous mutations in the same transcription factor, GATA2, accounting for their disease.

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This page was last updated on Tuesday, August 10, 2021

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